TLRs Sample Clauses

TLRs. Similar to other pathogens, RV expresses pathogen-associated molecular patterns (PAMPs) capable of binding PRRs and activating protective signaling. Up to 2 days post inoculation of IECs to RV, upregulation of TLR2, 3, 7, and 8 was observed (27). This pattern of TLR upregulation was also observed in peripheral blood mononuclear cells (PBMCs) of children infected with RV. Up to 3 days after illness onset, PBMCs upregulated TLR2, 3, 4, 7, and 8 with TLR3 and 8 remaining upregulated long after illness onset (28). Neither study addressed the consequence of TLR involvement, however, both demonstrated potential roles for a variety of TLRs during infection. TLR3, a sensor for dsRNA, has been more thoroughly investigated during RV infection. In vivo exposure to RV-derived dsRNA induced IEC apoptosis, prevented timely cellular repair, and provoked IL-15 production thought to attract natural killer (NK) cells to the site of infection (29, 30). Such TLR3 expression and signaling could be considered somewhat beneficial to the host. Despite a protective role for TLR3, a more recent study demonstrated a much different finding; Xxxx and colleagues found that TLR3 expression is limited in mice most susceptible to infection, and thus TLR3 is incapable of participating in a protective response (31). Clearly, more research is needed to define which TLRs control of RV infection and influence immunity during infancy and beyond.
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